Search PubMed⌕ Search

Biomedical subjects

B S Gan

Publications and source records attributed to B S Gan.

25 records · Page 2Linked to original sources
PubMed1994

An unusual complication of appendectomy.

Intraabdominal abscess formation is a well-recognized complication of perforated appendicitis. Extraabdominal complications, however, are rare. The authors present the case of an 8-year-old boy who had an acute painful right-sided scrotal mass 2 days after an operation for perforated appendicitis. During exploration, an abscess within a previously undiagnosed patent processus vaginalis was found and successfully managed by drainage. This case demonstrates that a persistent patent processus vaginalis may predispose to scrotal pathology secondary to intraabdominal sepsis and represents a unique complication of perforated appendicitis.

Abscess↗
PubMed1990

Distinct coronary artery receptor systems for epidermal growth factor-urogastrone.

In porcine (PCA) and bovine (BCA) coronary arterial strips, epidermal growth factor-urogastrone (EGF-URO) caused an endothelium-independent Ca-requiring contractile response that could not be attributed to the secondary release of agonists from neural elements. In these tissues, EGF-URO also potentiated the contractile actions of other agonists (prostaglandin F2 alpha, KCl or norepinephrine). Nonetheless, the responsiveness of the PCA and BCA preparations differed markedly in terms of 1) their sensitivity to indomethacin and dexamethasone (indomethacin and dexamethasone abrogated the PCA but not the BCA response), 2) their desensitization properties (the BCA rapidly desensitized, whereas the PCA did not) and 3) the order of potencies for EGF-URO and transforming growth factor-alpha (TGF-alpha) (in the PCA, EGF-URO was more potent than TGF-alpha, whereas in the BCA, the potency of TGF-alpha was greater than or equal to that of EGF-URO). Taken together our data document the presence of two distinct receptor signaling systems for EGF-URO in the PCA and BCA preparations, and our results support the hypothesis that distinct receptor subtypes for EGF-URO may be present in these two tissues.

Animals↗
PubMed1989

Autoradiographic localization of binding sites for epidermal growth factor-urogastrone (EGF-URO) in coronary arteries.

Previously published data have indicated that epidermal growth factor-urogastrone (EGF-URO) can regulate blood flow in vivo and can modulate vascular smooth muscle contractility in vitro. However, the exact location of the receptors responsible for this vascular action of EGF-URO has not been previously determined. In this report, employing in vitro autoradiography with 125I-labeled EGF-URO, we have documented the presence of specific EGF-URO binding sites in the tunica media of bovine and porcine coronary arteries. Our observations support the indirect evidence pointing to presence of EGF-URO receptors on the smooth muscle elements of arterial tissue. Our data also support further the hypothesis that EGF-URO and related growth factors (like TGF-alpha or PDGF) may play a role in normal and pathophysiological vascular function.

Animals↗
PubMed1987

Epidermal growth factor-urogastrone causes vasodilatation in the anesthetized dog.

Epidermal growth factor-urogastrone (EGF-URO) administered intraarterially was a potent dilator in dog femoral (FEM), superior (cephalic) mesenteric (SMA), celiac (CAC), coronary (COR), carotid (CAR), and renal (REN) vascular beds. The effects of EGF-URO, which exhibited tachyphylaxis, could not be attributed either to recirculating EGF-URO or to the secondary release of other agonists or products of the cyclooxygenase pathway. Two vascular beds (FEM, SMA) showed a high maximum responsiveness to EGF-URO (maximum effect [Emax] approximately equal to 70% increase in flow) whereas another group (CAC, COR, CAR, and REN) exhibited lower responsiveness (Emax approximately equal to 20%). The ED50 for this effect of EGF-URO was in the range of 0.4 micrograms (FEM, SMA, CAR, and COR) to 0.9 micrograms (CAC and REN). In isolated dog COR helical strips, EGF-URO did not exhibit either a direct relaxing or a contractile effect. However, preincubation of strips with EGF-URO caused up to a 66% inhibition of contraction in response to norepinephrine (1 microM), with an ED50 for EGF-URO of 1 nM. This action of EGF-URO also showed marked tachyphylaxis. Our data point to a potential role for EGF-URO (and possibly for the structurally related alpha-transforming growth factor) in the regulation of blood flow in vivo.

Animals↗
PubMed1987

Distinct vascular actions of epidermal growth factor-urogastrone and transforming growth factor-alpha.

We compared the effects of epidermal growth factor-urogastrone (EGF-URO) with those of transforming growth factor-alpha (TGF-alpha) on regional blood flow in the anesthetized dog in vivo, and on isolated canine helical coronary artery strips in vitro. Like EGF-URO, TGF-alpha was a potent stimulator of femoral arterial blood flow in vivo; and, when added to the tissue bath in vitro before an agonist, TGF-alpha like EGF-URO was a potent inhibitor of the contractile responses of helical coronary arterial strips to various smooth muscle agonists: norepinephrine (NE), prostaglandin F2 alpha (PGF alpha) and potassium chloride (KCl). Nonetheless, there were marked differences between EGF-URO and TGF-alpha in terms of the two biological responses measured. In terms of blood flow, although the ED50 for the increase in blood flow was similar for EGF-URO and TGF-alpha (ED50 = 0.4 micrograms EGF-URO equivalents per dose), the maximum responsiveness to TGF-alpha (130% increase in flow) was substantially greater than the maximum response to EGF-URO (70% increase in flow). Furthermore, TGF-alpha did not cause tachyphylaxis to subsequent doses of TGF-alpha, whereas a prior dose of either EGF-URO or TGF-alpha desensitized markedly the blood flow preparations to EGF-URO. Different desensitization patterns for the actions of EGF-URO and TGF-alpha also were observed in the arterial strip preparations. The inhibitory action of EGF-URO for agonist (NE, PGF2 alpha or KCl)-mediated contraction was diminished with repeated exposure of the tissue to EGF-URO, whereas the inhibitory action of TGF-alpha persisted with repetitive tissue exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗